10.3 Candidacy, outcomes, and closing the book

Four clinical populations form the routine candidacy for bone-conduction devices. Each exploits one of the BCD’s distinctive properties — bypassing a non-functional conductive apparatus, routing sound from a deaf ear via the skull to the working contralateral cochlea, or accommodating anatomy that cannot host a conventional ear-canal-worn device.

1. Bilateral conductive or mixed losses with good cochlear reserve

Patients with bilateral conductive or mixed sensorineural-conductive losses are the classical BCD population. The conductive component is bypassed entirely by the device; the cochlea, if its bone-conduction thresholds are good (≤ 25 dB HL average), responds well. Examples:

• Chronic otitis media with bilateral effusion or perforations that resist surgical repair.
• Congenital ossicular fixation (rare).
• Bilateral otosclerosis in patients who are poor candidates for stapedectomy.
• Post-mastoidectomy patients with surgically modified middle-ear anatomy.

Expected outcomes: aided thresholds close to the patient’s bone-conduction thresholds (typically 15–25 dB HL). Speech-in-quiet > 90%. Speech-in-noise dependent on the residual cochlear reserve.

2. Single-sided deafness (SSD)

Patients with unilateral profound or total hearing loss in one ear and normal or near-normal hearing in the other are increasingly common BCD candidates. The bilateral-skull-conduction property is the key: a BCD on the deaf side transmits sound through the skull to the working contralateral cochlea, restoring awareness of acoustic input from the deaf side.

What the BCD cannot restore in SSD: true binaural cues. The deaf cochlea is still non-functional; the working contralateral cochlea is receiving both its own ipsilateral input and the BCD’s contralateral input via bone, but with no differentiation that would support spatial localisation or stream segregation. The BCD addresses head-shadow problems (someone speaking on the deaf side is now audible) but does not restore stereo hearing.

Alternative: CROS (contralateral routing of signal) hearing aid. The CROS uses a microphone on the deaf side and a wireless link to a receiver on the good side, which delivers the signal acoustically into the good ear canal. CROS is non-surgical, lower-cost, and has similar functional outcomes to BCD for SSD. The clinical choice between CROS and BCD for SSD depends on cosmetic preference, ear-canal occlusion sensitivity (the CROS receiver occludes the good ear; the BCD does not), and patient adherence.

A more recent option for SSD is the cochlear implant in the deaf ear — providing actual binaural input rather than ipsilateral routing. CI for SSD has been FDA-approved since 2019 and is rapidly displacing BCD and CROS in centres with strong CI programs. The decision tree for SSD increasingly is: try a BCD or CROS on a trial basis; if outcomes are unsatisfactory and the deaf cochlea is anatomically suitable, proceed to CI in the deaf ear.

3. Congenital aural atresia or microtia

Children born with aural atresia (absent ear canal) or microtia (malformed pinna) have no acoustic pathway in the affected ear regardless of cochlear health. Most have normal cochlear function — the cochlea developed normally, but the external/middle ear failed to form. These children are obligate BCD candidates from infancy.

Pediatric BCD fitting follows a standard protocol:

• Birth–6 months: identification via newborn hearing screening (AABR — Ch 6). Acoustic immittance testing not informative because the canal is absent. Bone-conduction ABR is the primary objective threshold tool.
• 6 months–2 years: BCD softband fitting. Both unilateral atresia (where the contralateral ear is normal) and bilateral atresia are fit, on the basis of the sensitive-period evidence and audibility considerations.
• Age 5+: surgical implantation candidate (BAHA, BAHA Attract, or Osia) if the parents and child consent and the contralateral ear remains an audiometric problem.

Unilateral atresia is more common than bilateral (~1 in 10,000 births vs 1 in 100,000). The clinical decision for unilateral atresia is whether to fit the impaired ear at all — the child has one normally-developing ear, after all, and unilateral hearing loss has historically been considered “acceptable” without intervention. Contemporary evidence (Lieu et al. 2010, 2014) has shifted the picture: unilateral hearing loss in childhood does produce measurable academic and speech-in-noise deficits relative to bilateral-normal-hearing peers, and BCD fitting in unilateral atresia is now routinely recommended.

4. Adults intolerant of in-the-ear devices

A small but real BCD population is adults with conductive or moderate sensorineural losses whose anatomy or physiology makes conventional in-the-ear or canal-worn hearing aids untenable. Chronic eczema or psoriasis of the ear canal, narrow canals from surgical scarring, post-radiation otitis externa, or recurrent severe otitis media may all preclude long-term canal-worn devices. A BCD provides a route to amplification without occluding the canal.

This population is small but the BCD genuinely offers them an option no other class of device can provide.

Outcomes summary

Pooled across the four candidacy populations, modern BCD users achieve:

Patient-reported benefit (APHAB, COSI questionnaires) is consistently positive across all candidacy populations, with reported benefit comparable to or slightly higher than conventional hearing aids for the matched-degree-of-loss conductive populations. The combination of objective audiometric improvement and high patient satisfaction has secured BCD’s clinical role.

Closing the book

Ten chapters in, the book has worked through the audiologist’s complete clinical toolkit:

• Chapters 1–3 developed the behavioural assessment tools: pure-tone audiometry, masking, speech audiometry. These tools establish what the patient can hear and how reliably they can discriminate speech — the functional starting point.
• Chapters 4–6 developed the objective assessment tools: tympanometry, acoustic immittance, otoacoustic emissions, evoked potentials. These tools localise pathology along the entire auditory pathway from canal to cortex without requiring patient cooperation, and they make universal newborn hearing screening possible.
• Chapters 7–10 developed the interventions: hearing aids (with their multichannel WDRC, directional microphones, and adaptive feedback cancellation), real-ear verification (the bridge between audiogram and well-fit device), cochlear implants (for cochlear damage beyond what amplification can compensate), and bone-conduction devices (for conductive losses and SSD).

The unifying mathematical and acoustic ideas — impedance and admittance, the Fourier filterbank, signal averaging, the SII as the audibility-to-intelligibility bridge, current spread along a cochlear electrode array, the closed-loop stability criterion that makes adaptive feedback cancellation possible — link the chapters into a coherent whole. The audiologist works at the intersection of acoustics, cochlear physiology, and signal processing; this book has tried to honour that intersection by treating each clinical tool as an applied instance of the underlying physics and math.

A book like this is, of course, a snapshot. The pace of change in audiology is accelerating: DNN-based hearing aid processing, gene therapy for genetic deafness, totally implantable hearing aids, brainstem and midbrain implants for patients without functional auditory nerves, regenerative therapies for cochlear hair cells. Each of these is in active clinical research as of 2026. Some will become standard of care; others will not. The fundamental tools — the audiogram, tympanogram, OAE, ABR, hearing aid, cochlear implant, BCD — have all been with us for decades, and the underlying physics and physiology will remain the framework against which any future technology gets understood. We have tried, throughout, to develop that framework as carefully as the clinical detail will allow.

Beyond the toolkit, the audiologist’s deepest skill is integration: synthesising audiogram + tympanogram + reflex + OAE + ABR + speech-in-noise + patient history into a coherent diagnostic picture, and then matching the appropriate intervention to the patient’s specific configuration. No single test answers the clinical question; their combination usually does. The book has worked through the components one at a time so that the audiologist-in-training can practice the synthesis — building the mental model that connects, say, a type-As tympanogram + low-frequency conductive loss + intact stapedial reflexes + an audiometric Carhart notch into the diagnosis of otosclerosis with a clear next-step plan.

That work — the diagnostic synthesis and intervention planning — is the audiology profession. The tools described here are its language.

— End of book.